Key result
Short-term water deprivation did not increase beat-to-beat systolic blood pressure variability compared to euhydration (1.9 vs. 1.8 mmHg; P=0.24) in healthy young adults.
Why the study?
Elevated plasma sodium from high dietary salt increases blood pressure variability in rodents, but whether water deprivation-induced serum sodium elevations augment blood pressure variability via baroreflex function and sympathetic vascular transduction in humans was unknown.
Does short-term water deprivation increase blood pressure variability or impair neurovascular function in healthy young adults?
RCT (n=35)
randomized crossover
Does short-term water deprivation increase blood pressure variability or impair neurovascular function in healthy young adults?
Short-term water deprivation modestly increases serum sodium but does not affect blood pressure variability or neurovascular function in healthy young adults.
Short-term water deprivation appears safe for BP variability in healthy young adults; challenges assumptions linking mild dehydration to autonomic impairment.
High dietary salt increases arterial blood pressure variability (BPV) in salt-resistant, normotensive rodents and is thought to result from elevated plasma [Na + ] sensitizing central sympathetic networks. Our purpose was to test the hypothesis that water deprivation (WD)-induced elevations in serum [Na + ] augment BPV via changes in baroreflex function and sympathetic vascular transduction in humans. In a randomized crossover fashion, 35 adults [17 female/18 male, age: 25 ± 4 yr, systolic/diastolic blood pressure (BP): 107 ± 11/60 ± 7 mmHg, body mass index: 23 ± 3 kg/m 2 ] completed two hydration protocols: a euhydration control condition (CON) and a stepwise reduction in water intake over 3 days, concluding with 16 h of WD. We assessed blood and urine electrolyte concentrations and osmolality, resting muscle sympathetic nerve activity (MSNA; peroneal microneurography; 18 paired recordings), beat-to-beat BP (photoplethysmography), common femoral artery blood flow (Doppler ultrasound), and heart rate (single-lead ECG). A subset of participants ( n = 25) underwent ambulatory BP monitoring during day 3 of each protocol. We calculated average real variability as an index of BPV. WD increased serum [Na + ] (141.0 ± 2.3 vs. 142.1 ± 1.7 mmol/L, P < 0.01) and plasma osmolality (288 ± 4 vs. 292 ± 5 mosmol/kg H 2 O, P < 0.01). However, WD did not increase beat-to-beat (1.9 ± 0.4 vs. 1.8 ± 0.4 mmHg, P = 0.24) or ambulatory daytime (9.6 ± 2.1 vs. 9.4 ± 3.3 mmHg, P = 0.76) systolic BPV. Additionally, sympathetic baroreflex sensitivity ( P = 0.20) and sympathetic vascular transduction were not different after WD ( P = 0.17 for peak Δmean BP following spontaneous MSNA bursts). These findings suggest that, despite modestly increasing serum [Na + ], WD does not affect BPV, arterial baroreflex function, or sympathetic vascular transduction in healthy young adults.
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Watso et al. (2019) conducted an RCT in healthy young adults (n=35). Water deprivation vs. Euhydration control condition was evaluated on Beat-to-beat systolic blood pressure variability (p=0.24). Short-term water deprivation did not increase beat-to-beat systolic blood pressure variability compared to euhydration (1.9 vs. 1.8 mmHg; P=0.24) in healthy young adults.
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